Cataracts, or lens opacities, are the leading cause of blindness worldwide. Cataracts are treatable with surgery, however, currently, no other therapies are available that could either inhibit, slow down, or reverse the development of cataracts. Therefore, it is necessary to expand our current knowledge of biological processes that lead to cataracts. The goals of this study are to develop mouse cataract models defined on molecular level that show how mutations in genes important for lens transparency correlate with functional, structural and biochemical abnormalities resulting in cataracts. [unreadable] This study focuses on two mouse cataract models of nuclear cataracts: coralliform cataract (Coc) is [unreadable] an autosomal dominant cataract that maps to 28.06 cM on mouse chromosome 16 in the region with synteny with HSA3q13-q21; lens opacity 4 (Lop4) is a semidominant nuclear cataract that maps to 96 cM on mouse chromosome 2 in the region of synteny with HSA20q11-q13. The specific aims of this study are: [unreadable] Specific Aim (1): Fine linkage map Coc and Lop4 loci to reduce the critical regions to < 1Mb. [unreadable] Specific Aim (2): Establish BAC minimal tiling path over Coc and Lop4 critical regions. [unreadable] Specific Aim (3): Identify and test positional candidate genes for causal association with the disease. [unreadable] Specific Aim (4): Once genes and mutations responsible for the Coc and Lop4 phenotypes are identified, the focus will be on characterizing the process of cataract development at the molecular level. [unreadable] [unreadable] [unreadable]